Joya D Pickett1, Elizabeth Bridges2, Patricia A Kritek2, JoAnne D Whitney2. 1. Joya D. Pickett is a critical care clinical nurse specialist at Swedish Medical Center, Seattle, Washington. Elizabeth Bridges is a professor at University of Washington School of Nursing and a clinical nurse researcher at University of Washington Medical Center, University of Washington Medicine, Seattle, Washington. Patricia A. Kritek is medical director of critical care and an associate professor in the Division of Pulmonary and Critical Care Medicine at University of Washington Medical Center. JoAnne D. Whitney is a professor at the University of Washington School of Nursing and endowed professor in critical care nursing at Harborview Medical Center, University of Washington Medicine. joyap@u.washington.edu. 2. Joya D. Pickett is a critical care clinical nurse specialist at Swedish Medical Center, Seattle, Washington. Elizabeth Bridges is a professor at University of Washington School of Nursing and a clinical nurse researcher at University of Washington Medical Center, University of Washington Medicine, Seattle, Washington. Patricia A. Kritek is medical director of critical care and an associate professor in the Division of Pulmonary and Critical Care Medicine at University of Washington Medical Center. JoAnne D. Whitney is a professor at the University of Washington School of Nursing and endowed professor in critical care nursing at Harborview Medical Center, University of Washington Medicine.
Abstract
BACKGROUND: Intravenous fluid boluses are administered to patients in shock to improve tissue hypoperfusion. However, fluid boluses result in clinically significant stroke volume increases in only about 50% of patients. Hemodynamic responses to passive leg raising measured with invasive and minimally invasive methods are accurate predictors of fluid responsiveness. However, few studies have used noninvasive blood pressure measurement to evaluate responses to passive leg raising. OBJECTIVE: To determine if passive leg raising-induced increases in pulse pressure or systolic blood pressure can be used to predict clinically significant increases in stroke volume index in healthy volunteers. METHODS: In a repeated-measures study, hemodynamic measurements were obtained in 30 healthy volunteers before, during, and after passive leg raising. Each participant underwent the procedure twice. RESULTS: In the first test, 20 participants (69%) were responders (stroke volume index increased by ≥ 15%); 9 (31%) were nonresponders. In the second test, 15 participants (50%) were responders and 15 (50%) were nonresponders. A passive leg raising-induced increase in pulse pressure of 9% or more predicted a 15% increase in stroke volume index (sensitivity, 50%; specificity, 44%). There was no association between passive leg raising-induced changes in systolic blood pressure and fluid responsiveness. CONCLUSION: A passive leg raising-induced change in stroke volume index measured by bioreactance differentiated fluid responders and nonresponders. Pulse pressure and systolic blood pressure measured by oscillometric noninvasive blood pressure monitoring were not sensitive or specific predictors of fluid responsiveness in healthy volunteers.
BACKGROUND: Intravenous fluid boluses are administered to patients in shock to improve tissue hypoperfusion. However, fluid boluses result in clinically significant stroke volume increases in only about 50% of patients. Hemodynamic responses to passive leg raising measured with invasive and minimally invasive methods are accurate predictors of fluid responsiveness. However, few studies have used noninvasive blood pressure measurement to evaluate responses to passive leg raising. OBJECTIVE: To determine if passive leg raising-induced increases in pulse pressure or systolic blood pressure can be used to predict clinically significant increases in stroke volume index in healthy volunteers. METHODS: In a repeated-measures study, hemodynamic measurements were obtained in 30 healthy volunteers before, during, and after passive leg raising. Each participant underwent the procedure twice. RESULTS: In the first test, 20 participants (69%) were responders (stroke volume index increased by ≥ 15%); 9 (31%) were nonresponders. In the second test, 15 participants (50%) were responders and 15 (50%) were nonresponders. A passive leg raising-induced increase in pulse pressure of 9% or more predicted a 15% increase in stroke volume index (sensitivity, 50%; specificity, 44%). There was no association between passive leg raising-induced changes in systolic blood pressure and fluid responsiveness. CONCLUSION: A passive leg raising-induced change in stroke volume index measured by bioreactance differentiated fluid responders and nonresponders. Pulse pressure and systolic blood pressure measured by oscillometric noninvasive blood pressure monitoring were not sensitive or specific predictors of fluid responsiveness in healthy volunteers.